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Nutrition 1 semester 2 > Lipids > Flashcards

Lipids Flashcards

1
Q

What is the % of fat in a lean healthy man vs severe obese

A

approx 16% compared to 70% mostly in adipocytes

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2
Q

What did the research of Ancel Keys find

A

High sat fat diet would increase serum cholesterol and lead to heart disease. The American Heart Assoc. then recommended a low fat high carb diet, substituting animal fats for seed oils. This led to into of statins.

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3
Q

Describe WHITE adipose fat and list functions

A

complex metabolically active endocrine tissue
- secretion of hormones
- growth factors
- enzymes
- protection of organs
- energy storage
- temperature insulation

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4
Q

Lipids exist in various forms, each with different structure and function. Name 4

A
  • individual fatty acids
  • triglycerides
  • phospholipids (every cell membrane)
  • cholesterol (steroid based compounds eg oestrogen)
  • Sphingolipids (in nerve cell membranes eg myelin)
  • Glycolipids (cell identity)
  • cerebrosides (in brain)
  • fat soluble vits (ADEK)
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5
Q

List as many function of lipids as you can (up to 10)

A
  • Energy production (1g fat = 9 calories)
  • storage of energy reserves (fats more efficient form of storage than carbs or proteins so excess stored as fat)
  • cell membrane structure
  • Thermal insulation (subcutaneous tissue around organs)
  • steroid hormones (e.g. progesterone/oestrogen)
  • formation of eicosanoids (signalling molecules involved in processes such as inflammation)
  • Growth and development (brain rich in AA/DHA)
  • Constitutes nervous tissue structure
  • cell to cell signalling
  • needed for absorption of ADEK
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6
Q

Describe the chemical structure of fatty acids

A

hydrocarbon chains with acid group at one end and methyl at other.

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7
Q

How many carbons does a short chain and medium chain fatty acids have, where do they travel to and what are they used for.
Which is useful to take before exercise

A

Short chain: 5 C
Medium chain: 6-12 Cs
Travel to liver used to create energy or ketones.
MCTs good source of energy before exercise (1tbs)

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8
Q

How many carbons does a long chain and very long chain fatty acid have and what are they used for

A

14-22 C and more than 22 Cs
Build cell membranes

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9
Q

How are SCFAs produced by the body

A

by dietary fibre fermenting in the COLON

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10
Q

Name the most common SCFAs

A

Acetate
Propionate
Butyrate

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11
Q

Which fatty acid is important for colon health and why

A

BUTYRATE
- supports intestinal tight junctions
- anti-inflammatory effect on the colon

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12
Q

How are fatty acids named

A

Using their common names and the omega nomenclature system
- Omega system: number of carbon atoms, number of double bonds, number of carbons from the omega end to the first carbon in the double bond.

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13
Q

How do unsaturated fats become saturated

A

with the addition of a hydrogen - hydrogenation, which turns the natural fatty acid into unnatural forms (trans)

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14
Q

Describe the composition of a saturated fatty acid (e.g. how many c-c double bonds)

A

no C-C double bonds. All carbons are completely saturated with hydrogen bonds.
Solid at room temperature

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15
Q

Describe the composition of unsaturated fatty acids

A

one or more double bonds between carbons. Liquid at room temp

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16
Q

Describe the composition of monounsaturated fatty acids

A

one double bond in the chain

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17
Q

Describe the composition of PUFAs

A

several double bonds in the

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18
Q

What is the result of an increasing number of double bonds in a fatty acid

A

the more double bonds the less stable and increasing susceptibility to oxidation

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19
Q

What do trans fats do to blood triglyceride and cholesterol profiles and what disease states are they linked to

A

alter blood triglyceride and cholesterol profiles - linked to CVD, insulin resistance and cancer.

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20
Q

Explain the configuration of a CIS fatty acid

A

H atoms are on the same side of the double bond

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21
Q

explain the configuration of a TRANS fat

A

H atoms are on separate sides of the double bond

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22
Q

are trans fats saturated or unsaturated

A

unsaturated but behave like saturated fats because of their unkinked shape

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23
Q

Name a natural trans fat

A

CLA - conjugated linoleic acid found in grass fed meat and dairy. Could increase lean muscle mass and decrease body fat.

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24
Q

Triglycerides: major form of dietary fat and storage form. Describe their structure

A

1 glycerol and three fatty acids.
The fatty acids can differ in length (number of C atoms) and degree of saturation (no. of hydrogen molecules attached)

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25
Q

What disease state is a high level of triglycerides linked to

A

atherosclerosis - heart disease and stroke

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26
Q

When does the body synthesise triglycerides
what is the process called
where are they taken up

A
  • when caloric intake exceeds energy requirements
  • Excess energy is converted to triglycerides via lipogenesis in the liver and adipose tissue
  • taken-up by adipose tissue
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27
Q

Where do adipocytes acquire triglycerides from

A

circulating lipoproteins, chylomicrons and VLDL

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28
Q

What is lipogenesis

A

The process of converting acetyl-CoA to triglycerides for storage in fat

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29
Q

when are fatty acids synthesised

A

when there is an excess of carbohydrates

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30
Q

what is acetyl-CoA formed from and how does it form palmitic acid

A

from glucose during glycolysis, as well as from fats and amino acids
- 2 carbon units are added to form palmitic acid (C16)
- 3 fatty acids are bound to glycerol and stored as triglycerides

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31
Q

where in the body does fatty acid synthesis take place

A

in the liver, adipocytes, kidneys, lactating mammary glands

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32
Q

LIPOLYSIS - when does it take place and what happens

A

When dietary energy in limited triglycerides are hydrolysed by LIPASE into fatty acids and glycerol for use in the body

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33
Q

What hormones stimulate lipolysis and what hormone antagonises the lipolytic effect of these hormones

A
  • adrenaline and noradrenaline (stress)
  • adrenocorticotropic hormone (ACTH)
  • Glucagon and growth hormones
  • TSH and thyroxine

Antagonised by insulin which leads to disregulated breakdown of triglycerides which congregate in central adipose tissue/visceral fat which is metabolically active, secreting inflammatory cytokines and creating cycle of insulin resistance

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34
Q

Describe the process of fatty acid catabolism to produce ENERGY

A
  • CARNITINE facilitates the transport of fatty acids across the mitochondrial membrane.
  • fatty acids undergo BETA OXIDATION and are broken down into 2-carbon blocks as ACETYL -CoA
  • Acetyl Co-A is oxidised via the krebs cycle to CO2 and H2O.
  • energy created in electron transport chain
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35
Q

KETOSIS when does it take place

A

when carbohydrate levels are low (below 40g/day), fat becomes the primary fuel for energy production rather than glucose. Ketones are synthesised as they can cross the BBB. Happens during periods of fasting

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36
Q

what is ketogenesis

A

acetyl-CoA is converted to
acetoacetate
b-hydroxybutyrate
acetone - which gives the sweet smell to breath

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37
Q

what are the health benefits of ketosis

A

weight loss, epilepsy management, parkinson, alzheimers

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38
Q

what is ketoacidosis

A

dangerous condition where there’s insufficient pancreatic insulin to regulate B-hydroxybutyrate (remember, insulin is antagonist to lipolysis; therefore uncontrolled breakdown of lipids leading to acidity)

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39
Q

How can we optimise the digestion of lipids

A
  • chew and don’t drink with meals
  • increase bile production and stomach acid levels, bitter foods. reduce stress
  • Choleretics (increase bile production); cholagogues (Increase bile flow) eg dandelion, turmeric)
  • increase glycine and taurine (components of bile) in legumes, spinach and eggs
    -Olive oil can stimulate bile secretion
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40
Q

Lipid digestion - Explain the process of triglyceride digestion and the key enzymes needed

A

Glycerol separated from fatty acids by:
- gastric lipase (stomach)
- pancreatic lipase (duodenum)

Bile emulsifies fat, increasing surface area of droplets.

the free fatty acids and glyceride are transported to enterocytes where rebuilt and packaged into CHYLOMICRONS and transported via lymphatic system to the bloodstream.

Fatty acids are used or stored in adipose tissue

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41
Q

Lipid recommendations: What % of total energy should
TOTAL fat be
SATURATED fat
PUFA
Omega 3

A

Total : 20-35% (44-78g based on 2k cal)
Saturated : no more than 10% (22g)
PUFA: 6-11% (13-24g)
Omega: .5-2% (1.1-1.4g)

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42
Q

What does the UK Government Scientific Advisory Committee on Nutrition advise regarding fat intake

A

Sat fat not to exceed 10% dietary intake of energy
Low fat dairy (oft high in sugar)
unsaturated oils and spreads (refined and trans fats)
NO emphasiss on healthy fats (fish, avocado, nuts, seeds, EVOO, egg yolk, grass fed meat)

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43
Q

Without adequate energy from fat, people aren’t satiated. What did the PURE 2017 study find regarding mortality and fat consumption

A

people consuming more than 35% of daily energy in fat less likely to die than those consuming 10%

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44
Q

List benefits of including healthy fats in diet (eg mix of mono, poly and sat fats including fat soluble vits such as E)

A

greater satiety
sources of EFAs
Choline (to synthesise phospatidylcholine)
source of ADEK and phytonurients
greater flavour enhancement of cooked food

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45
Q

List food sources of healthy dietary fats

A

fruit - avo, olives
seeds - chia, flax, hemp, pumpkin
nuts - almonds, brazils, walnuts
COLD PRESSED seed oils - flax, chia, olive, sunflower
Oily fish - SMASH

46
Q

Saturated fats : how does the body use the MCT (medium chain triglycerides) in coconut oil

Name the fat contained in 50% of coconut oil and its benefits
What diseases do they potentially help

A

as a source of fuel, or turns them into ketones.

MCTs increase the number of calories burned compared to longer chain fatty acids

Lauric acid, which can form monolaurin. Both are antebacterial, antiviral, antifungal.
Increase HDL and lower LDL

Positive outcomes in epilepsy, and alzheimers

47
Q

Name the SATURATED fats and the food they’re found in

A

Butyric acid (4C) - dairy. produced in gut

Caprylic acid (8-c) - coconut, palm kernal, breast milk. Antifungal

Lauric acid (12-c) - coconut

Palmitic acid - coconut, palm, palm kernal

Stearic acid (18-c) - beef, pork, lamb, cocoa, shea butter and butter

48
Q

Name the MONOunsaturated fats and foods found in (x2)

A

Palmitoleic acid Omega 7: coconut, palm kerbal, macadamia nuts

Oleic acid omega-9: olive, avocado, almond, peanut, pistachio, brazil, pecan, cashew, animal fat, butter, hazlenut, neem, macadamia

49
Q

Name the POLYUNSATURATED FATS and food sources

A

OMEGA 3
ALPHA- LINOLENIC ACID ALA)
flaxseed (richest source), chia, hemp, dark green leaves, Pumpkin seed, rapeseed, walnuts

STEARIDONIC ACID (SDA)
Blackcurrent seed

EPA and (20 C, 5 dble bonds)
DHA (22 C, 6 dble bonds)
oily fish
spirulina and chlorella
DHA - marine algae

OMEGA 6
LINOLEIC ACID
Sunflower, hemp, soybean, walnut, avocado, brazilnut, pumpkin seed, chia, almond

GAMMA LINOLENIC ACID
evening primrose, borage oil, blackcurrent seed

ARACHIDONIC ACID
meat and animal products

50
Q

name fats that can tolerate being heated and are preferable for cooking and why

A

coconut, ghee, butter - saturated.
More stable due to lack of double bonds

51
Q

why should you avoid frying foods

A

free radical formation

52
Q

How should monounsaturated fats be used for cooking and name some

A

extra virgin olive oil, avocado oil - not about 180; oxidise at higher temps but naturally occuring anti oxidants make them safer to use

53
Q

how should polyunsaturated fats be used during cooking and name two

A

veg and flaxseed oils
oxidise when heated and produce free radicals, so only used in raw cold pressed form
store in dark bottles in fridge or freezer
Look for pressing and used by date

54
Q

How do the fatty acids within triglycerides and unsaturated fatty acids go rancid

A

Fatty acids within triglycerides go rancid by releasing the fatty acids from glycerol
Unsaturated fatty acids within the triglycerides go rancid when the double bonds are oxidised

55
Q

What makes fats more prone to oxidation

A

if high in PUFA
exposed to prolonged heat light or O2
naturally low in antioxidants
refined or heavily processed.

56
Q

What products are formed from fat breakdown and rancidity.
What is generally formed from the oxidation of the double bonds in lipids

A

aldehydes, ketones, hydrocarbons
MALONDIALDEHYDE - it’s a mutagen found in hydrogenated or overheated fats.

57
Q

What is the name of the enzyme that catalyses the chemical reaction to produce GLA and EPA from ALA and LA

A

Delta-6-desaturase

58
Q

What is the ratio of Omega 6:3 in a western diet

A

16:1

59
Q

Why are EPA and DHA considered conditionally essential nutrients

A

due to the low conversion of ALA to EPA and DHA

60
Q

what is the recommended weekly intake in mg of EPA/DHA and how can it be achieved

A

250mg
2-3 portions of oily fish or algal source

61
Q

List functions of EFAs

A

maintain cell membrane fluidity, including organelle membranes
act with cell membrane proteins affecting transport of substances in and out of cell
cell to cell communication
foetal and child BRAIN development
precursor of eicosanoids (local hormones)

62
Q

List clinical indicators of low EFAs
Skin
Endocrine
Reproductive system
circulatory
muscoskeletal
immune
neurological

A

Skin: dry, flaky, chapped lips. Hyperkeratosis pilaris. delayed healing, dry brittle nails, acne, eczema, dermatitis, dry oily hair

Endocrine: weight imbalance, PMS, hyperinsulinaemia

Reproductive: infertility, miscarriages, ovarian cysts

circulatory: frequent nosebleeds, bleeding gums, easy bruising

Muscoskeletal: chronic joint pain/artiritis, delayed injury recovery

Immune: susceptibility to infections

Neurological: demential, alzheimers, parkinson, irritability, tingling, CFS

63
Q

Omega 3 - alpha linolenic acid. name food sources and how many carbons

A

flaxseeds, hemp seeds, soybeans, walnuts, dark green leaves

18 carbon

64
Q

List therapeutic uses of ALA

A

CVD - decrease risk of atherosclerosis; reduce C reactive protein levels; anti arrhythmic effect; anti-hypertensive - lowers activity of ACE (angiotensin converting enzyme); lowers LDL

Neurological: INCREASES BDNF (brain derived neurotropic factor… neuroprotective): BDNF supports strokes, promotes vasodilation in the brain; BDNF supports depression learning and memory

Anti-inflammatory: helpful in IBD, asthma and autoimmune conditions. But needs to be converted to EPA and DHA

65
Q

What are the drug interactions of ALA

A

it’s anti-coagulant. blood thinning meds eg warfarin and aspirin
cholesterol lowering meds (statins) - may have agonist effect when combined with statins

66
Q

Therapeutic uses of EPA and DHA x4 and supplemental dosage

A

CVD:
supplementation can significantly reduce blood triglyceride levels; lower BP; preventative against atherosclerosis and lowers blood fibrinogen levels. DART trial showed reduction in myocardial reinfarction after daily 900mg EPA/DHA
DOSAGE: 0.8 - 3g/day

Anti-infammatory:
inhibit NFkB, TNF-a and Interleukin-6. useful for arthritis, IBD, eczema, SLE.
>2.7g/day fish oils lowers NSAID use in arthritis people
DOSAGE: EPA 3-5g/day
`DHA 0.8-2.7g/day

Neurological health:
neuroprotective properties and increase BDNF. Lower levels associated with learning and behavioural problems.
Depression ADHD, alzheimers
DOSE:
EPA 0.6-3g
DHA 0.15-2g/day

Foetal health:
foetal brain development. Supplementation in pregnancy may protect children against allergies
DOSE: EPA 800mg/day
DHA 400mg/day

67
Q

Can a vegetarian diet meet EPA/DHA needs

A

yes by including good sources of ALA - flax/hemp seed
Support conversion by increasing enzyme co-factors (Zn, Mg, B6)
Moderate Omega 6
Algal EPA/DHA supps

68
Q

What might determine the quality of vegan omega oil quality

A

use of water extraction methods to provide DHA
Free from carrageenan which may induce inflammation in colonic cells
cold pressed, organic

69
Q

what might determine the quality of omega fish oil

A

sustainability practices
independently tested for purity and toxins
EPA and DHA content should be listed

70
Q

OMEGA 6
Linoleic Acid (LA)
what is the configuration

A

18:2 n-6

71
Q

Name food sources of LA

A

safflower, veg oils, sunflower, soybean, corn oils, nuts, seeds, some vegetables

72
Q

What vits/minerals does the conversion of LA to GLA require

A

C, B3, B6, Mg, Zn

73
Q

Why are flax and hemp seeds considered nutritionally superior to safflower?

A

they also contain omega 3 as well as 6

73
Q

Gamma-linolenic acid (GLA)
what is the configuration

A

18:3 n-6

74
Q

what are the main food sources of GLA

A

evening primrose oil, borage oils, hemp, blackcurrant seed oil

75
Q

List three therapeutic uses of GLA

A

Rheumatoid artirhtis
reduces pain, swelling and morning stiffness.
DOSEAGE: 1.4g/day of borage seed oil

ADHD: with EPA shows improvements in impulsiveness and attention

Eczema: reduced inflammation - improves skin symptoms
DOSAGE: 320mg GLA/day BUT be careful not to raise levels of AA

76
Q

List therapeutic uses of Evening Primrose Oil and which omega is it abundant in

A

Linoleic Acid (but also contains GLA)

PMS: GLA is precursor to PG1 which inhibits prolactin (high in women with PMS)
DOSE: 1500mg/day for 3 months

Cyclical mastalgia (breast pain): GLA forms PG1 which inhibits the synthesis of AA metabolites (therefore anti-inflammatory)
DOSE: 1000mg 3x daily 4-6 months

Female fertility: increases and optimises cervical mucus to sustain sperm during conception
DOSe: 1500-2000mg daily from day 1 of menses

77
Q

Name drug interactions of GLA

A

Ceftazidime - may increase effectiveness
Chemo - increase treatment effects
NSAIDs - counteract effects of GLA

78
Q

Arachidonic Acid (AA) where is it predominantly found

A

animal products, meat eggs dairy, esp when fed grain

79
Q

Arachidonic acid is seen as inflammatory. However, there are benefits and ways it which it is controlled. Explain…
What does PG2 do

A

Inflammation is an important part of the immune system’s response to injury and infection.

AA is metabolised by COX-1 and LOX-2 enzymes to prostaglandin series 2 (PG2).
PG2 causes inflammatory effects e.g. fever, vascular permeability, vasodilation, pain and oedema.

To prevent excess inflammation, PG2 induces 15-LOX activity that leads to formation of anti inflammatory lipoxins

80
Q

What are Eicosanoids (name some) and what are they formed from

A

formed from the oxidation of Omega 3 and 6 fats.
Locally acting hormone-like signalling molecules.
They include prostaglandins, leukotrienes, thromboxanes, resolvins and protectins

81
Q

What functions are eicosanoids involved in

A

Can be both pro and anti inflammatory

Inflammation
BV permeability and constriction
blood coagulation
Immune cell behaviour
lipid accumulation
CNS signalling

82
Q

How are eicosanoids formed; name the enzyme needed; what EFAs can they be made from

A

fatty acids are released from the membrane phospholipids by enzyme PHOSPHOLIPASE A2

COX and LOX convert them to eicosanoids (and then leukotrienes / prostaglandins etc depending on the starting fatty acid)

Made from AA, EPA DGLA

83
Q

Prostaglandins, made from eicosanoids, fall into three families/series, depending on which fatty acid they are made from.
Name which fatty acid Series 1 prostaglandin (PG1) is made from; is it pro or anti inflammatory, and its key functions

A

DGLA (dihomo-y-linolenic acid)
ANTI inflammatory
keeps blood platelets from sticking together
removes excess sodium and water from the body
relax blood vessels promoting circulation

84
Q

Prostaglandins, made from eicosanoids, fall into three families/series, depending on which fatty acid they are made from.
Name which fatty acid Series 2 prostaglandin (PG2) is made from; is it pro or anti inflammatory, and its key functions

A

AA
PRO inflammatory
promotes platelet aggregation
promotes sodium and water retention (increase BP)
oppose functions of PG1)

85
Q

Prostaglandins, made from eicosanoids, fall into three families/series, depending on which fatty acid they are made from.
Name which fatty acid Series 3 prostaglandin (PG3) is made from; is it pro or anti inflammatory, and its key functions

A

EPA
ANTI inflammatory
some have weak platelet aggregating properties
prevent release of AA from cell membranes
EPA is the most important factor limiting PG2 production

86
Q

How do the eicosanoids/prostaglandins work together to control inflammation

A

PG2 (Eicosanoids from from Arachidonic Acid) produce initial inflammation. This is shut off by eicosanoids made from DGLA and EPA - PG1 and PG3

87
Q

Why must the omegas be balanced

A

because the most abundant will occupy the enzyme active site, determining which prostaglandins will predominate. e.g. high AA = high PG2 = pro inflammatory.
High EPA/DHA = immune suppression

88
Q

Which Omega fatty acids can be affected by genetic variability

A

EPA and DHA
Polymorphisms are common in the genes coding for delta-6 and delta-5 desaturase. These are needed for the conversion of LA and ALA

89
Q

What factors/minerals might inhibit delta-6-desaturase and delta-5-desaturase

A

zinc, stress, insulin resistance, alcohol

90
Q

What are the common EFA tests

A

Omega-3 index: a marker for CV risk
Omega 6:3 ratio: a marker for chronic illness
AA:EPA ratio : a marker of ‘silent’ inflammation

91
Q

How can Omega 6:3 ratio be balanced with supplementation

A

supplement with EPA/DHA and address co-factor deficiencies needed for interconversion.

92
Q

List fatty acid profile tests

A

Genova - EFA and metabolic fatty acids (blood test)
Wiley’s Finest - omega-3 index test (blood spot)
Igennus - Opti-O-3 (blood spot)

93
Q

What is cholesterol essential for the synthesis or action of

A

Important for cell structure and function.

Vitamin D and Ca metabolism
Cortisol and related hormones
Alsosterone - for mineral and fluid balance
sex hormones
bile salts and acids
membrane integrity - esp the brain
Lipoproteins - needed for triglyceride and cholesterol transport.

94
Q

Where is cholesterol synthesised and excreted

A

DIETARY CHOLESTEROL DOESN’T MAKE A BIG DIFFERENCE IN PLASMA CHOLESTEROL LEVELS….
a triglyceride rich diet IS MORE PROBLEMATIC and stimulates cholesterol synthesis in the LIVER and SMALL INTESTINE, whereas dietary cholesterol is only partially absorbed.
Excreted in the stool intact, mostly as bile products

95
Q

What factors can help control levels of dieatry cholesterol

A

Fibre/non-digestible carbs increases the excretion of cholesterol
healthy microbes metabolise cholesterol leading to less reabsorption.
DIETARY CHOLESTEROL DOES NOT SIGNIFICANTLY AFFECT plasma cholesterol levels - its genetics and other nutritional factors such as high triglycerides

96
Q

Explain what HDL, LDL and VLDL are

A

they are lipoproteins, carriers of cholesterol and substances such as CoQ10, beta-carotene, Vit E.

LDL - takes cholesterol from liver to cells
VLDL - takes triglycerides to cells
HDL - carries cholesterol from cells back to liver

97
Q

How has the belief that cholesterol causes heart attacks been challenged

A

2009 study found ‘bad’ cholesterol was lower in people with heart disease
Over 10 years the % of men aged 65-74 with high cholesterol dropped from 87-54 whilst CHD remained at 20%

98
Q

What is the definition of low plasma cholesterol

A

it was 6.5 mmol/L but in 2004 dropped to below 5 mmol/L

99
Q

What is the role of cholesterol in atherosclerosis

A

Atherosclerosis is an inflammatory disease - no inflammation or injury to the endothelium, cholesterol doesn’t deposit. Look at high blood pressure or diabetes etc causing damage in the first place.
LDL cholesterol deposits in arterial wall and becomes oxidised.

100
Q

Which is a better means of measuring LDL - total cholesterol or measuring particle size

A

measuring particle size.
LDL: If LDLs are small and dense, 3x greater risk of coronary artery disease. Large and fluffy may be protective

HDL: larger HDLs more effective at removing cholesterol from blood and promote NO production in endothelial cells - anti-inflammatory and anti-thrombotic

101
Q

What might an increase in cholesterol indicate

A

A greater demand for cholesterol’s anti inflammatory function/need to repair cell membranes/make hormones etc.

102
Q

Cardiovascular markers. Explain the below:
Lipoprotein (a)
Lp-PLA2
Fibrinogen
C-reactive protein
Lipid peroxides

A

Lipoprotein (a): blood clotting agent. Key genetic risk factor in coronary artery disease.

Lp-PLA2: enzyme that plays a role in endothelial inflammation and atherosclerosis

Fibrinogen: raised levels are risk for clot formation

C-reactive protein: Inflammatory marker associated with CVD

Lipid peroxides: raised levels reflect oxidative damage to membranes.

103
Q

List cardiovascular markers

A

Lipoprotein (a)
Lp-PLA2
Fibrinogen
C-reactive protein
Lipid peroxides

104
Q

What are the ranges for serum cholesterol and triglycerides in GP tests

A

Serum cholesterol above 5 mmol/L = statins prescribed
Triglycerides optimal range is 0.79-1.24 mmol/L

105
Q

PHOSPHOLIPIDS/PHOSPHATIDES - structural basis of all cell membranes. What are they made up of and name three

A

Phosphatides: contain glycerol and 2 longchain fatty acids.
Inositol
choline
serine

106
Q

What is the role of lecithin

A

A group of fats, main source of choline. Synthesised by the liver and plays role in emulsification (fat digestion), increases solubility of cholesterol, improves cognitive function. Used to treat high cholesterol.

107
Q

Inositol is a key phospholipid - name therapeutic uses

A

Improves insulin sensitivity - used for insulin resistance, T2DM, PCOS, anxiety, chronic fatigue

108
Q

Phosphatidylserine is a key phospholipid - name therapeutic uses

A

Improves neuronal membrane functioning and cognitive function. Can be used for depression, insomnia, stress.

109
Q

Phosphatidylcholine is a key phospholipid - name therapeutic uses

A

neuro- and hepato-protective. Supplies choline for the synthesis of the neurotransmitter acetylcholine.
Memory, cognition, immunity, hormone function.

110
Q
A
111
Q

Name two foods containing the fat soluble vitamin E

A

Sunflower seeds
Almonds

Nutrition 1 semester 2 (11 decks)

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